The Medial Prefrontal Cortex-Basolateral Amygdala Circuit Mediates Anxiety in Shank3 InsG3680 Knock-in Mice.
10.1007/s12264-024-01280-5
- Author:
Jiabin FENG
1
;
Xiaojun WANG
1
;
Meidie PAN
2
;
Chen-Xi LI
1
;
Zhe ZHANG
1
;
Meng SUN
1
;
Tailin LIAO
2
;
Ziyi WANG
3
;
Jianhong LUO
1
;
Lei SHI
4
;
Yu-Jing CHEN
5
,
6
;
Hai-Feng LI
7
;
Junyu XU
8
Author Information
1. Department of Rehabilitation of Children's Hospital and School of Brain Science and Brain Medicine, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, 310003, China.
2. Liangzhu Laboratory, MOE Frontier Science Center for Brain Science and Brain-machine Integration, State Key Laboratory of Brain-machine Intelligence, Zhejiang University, Hangzhou, 311121, China.
3. Innovative Institute of Basic Medical Sciences of Zhejiang University (Yuhang), Hangzhou, 310058, China.
4. JNU-HKUST Joint Laboratory for Neuroscience and Innovative Drug Research, Jinan University, Guangzhou, 510632, China.
5. Department of Traditional Chinese Medicine, Xuanwu Hospital of Capital Medical University, Beijing, 100053, China. tcmcyj@
6. com.
7. Department of Rehabilitation of Children's Hospital and School of Brain Science and Brain Medicine, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, 310003, China. 6199005@zju.edu.cn.
8. Department of Rehabilitation of Children's Hospital and School of Brain Science and Brain Medicine, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, 310003, China. junyuxu@hkust-gz.edu.cn.
- Publication Type:Journal Article
- Keywords:
Anxiety;
Autism spectrum disorder;
Basolateral amygdala;
Medial prefrontal cortex
- MeSH:
Animals;
Prefrontal Cortex/metabolism*;
Basolateral Nuclear Complex/metabolism*;
Mice;
Anxiety/metabolism*;
Nerve Tissue Proteins/genetics*;
Male;
Gene Knock-In Techniques;
Pyramidal Cells/physiology*;
Mice, Transgenic;
Neural Pathways/physiopathology*;
Mice, Inbred C57BL;
Microfilament Proteins
- From:
Neuroscience Bulletin
2025;41(1):77-92
- CountryChina
- Language:English
-
Abstract:
Anxiety disorder is a major symptom of autism spectrum disorder (ASD) with a comorbidity rate of ~40%. However, the neural mechanisms of the emergence of anxiety in ASD remain unclear. In our study, we found that hyperactivity of basolateral amygdala (BLA) pyramidal neurons (PNs) in Shank3 InsG3680 knock-in (InsG3680+/+) mice is involved in the development of anxiety. Electrophysiological results also showed increased excitatory input and decreased inhibitory input in BLA PNs. Chemogenetic inhibition of the excitability of PNs in the BLA rescued the anxiety phenotype of InsG3680+/+ mice. Further study found that the diminished control of the BLA by medial prefrontal cortex (mPFC) and optogenetic activation of the mPFC-BLA pathway also had a rescue effect, which increased the feedforward inhibition of the BLA. Taken together, our results suggest that hyperactivity of the BLA and alteration of the mPFC-BLA circuitry are involved in anxiety in InsG3680+/+ mice.
